Author
Gianluca Luigi Russo
Bio: Gianluca Luigi Russo is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Reprogramming & Proteome. The author has an hindex of 4, co-authored 4 publications receiving 359 citations.
Topics: Reprogramming, Proteome, Astrocyte, Neurogenin-2, Mitochondrion
Papers
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TL;DR: Co-expression of Bcl-2 and anti-oxidative treatments leads to an unprecedented improvement in glial-to-neuron conversion after traumatic brain injury in vivo, underscoring the relevance of these pathways in cellular reprograming irrespective of cell type in vitro and in vivo.
268 citations
TL;DR: Key cell-intrinsic molecular and metabolic constraints that influence the establishment of a new identity as well as environmental inputs from injured brains that favor or harm the conversion process are discussed.
127 citations
TL;DR: A stab wound injury covering an entire neocortical column and targeted local reactive astrocytes via injecting FLEx switch (Cre-On) adeno-associated viral (AAV) vectors into mGFAP-Cre mice resulted in high-efficiency reprogramming of targeted astroCytes into neurons that develop lamina-specific hallmarks, including the appropriate long-distance axonal projections.
94 citations
TL;DR: The comprehensive mitochondrial proteome of cortical astrocytes and neurons is determined, identifying about 150 significantly enriched mitochondrial proteins for each cell type, including transporters, metabolic enzymes, and cell-type-specific antioxidants.
31 citations
Cited by
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Columbia University1, University of Pittsburgh2, Florey Institute of Neuroscience and Mental Health3, Stanford University4, German Cancer Research Center5, Ludwig Maximilian University of Munich6, Yale University7, Memorial Sloan Kettering Cancer Center8, Dresden University of Technology9, Wistar Institute10, National University of Mar del Plata11, University of Texas Health Science Center at San Antonio12, Guangzhou Medical University13, University of Connecticut Health Center14, Nagoya University15, New York University16, University of Arizona17
TL;DR: The mechanisms underlying ferroptosis are reviewed, connections to other areas of biology and medicine are highlighted, and tools and guidelines for studying this emerging form of regulated cell death are recommended.
3,356 citations
Lorenzo Galluzzi1, Lorenzo Galluzzi2, Ilio Vitale3, Stuart A. Aaronson4 +183 more•Institutions (111)
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
Abstract: Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.
3,301 citations
TL;DR: It is suggested that metallothionein (MT)‐1G is a new regulator of ferroptosis in HCC cells and enhances the anticancer activity of sorafenib in vitro and in tumor xenograft models.
412 citations
01 Jul 2004
TL;DR: It is demonstrated that distinct genetic programs operate at different stages of corticogenesis to specify the properties shared by all neocortical neurons.
Abstract: Neocortical projection neurons, which segregate into six
cortical layers according to their birthdate, have diverse
morphologies, axonal projections and molecular profiles,
yet they share a common cortical regional identity and
glutamatergic neurotransmission phenotype. Here we demonstrate
that distinct genetic programs operate at different
stages of corticogenesis to specify the properties shared
by all neocortical neurons. Ngn1 and Ngn2 are required to
specify the cortical (regional), glutamatergic (neurotransmitter)
and laminar (temporal) characters of early-born
(lower-layer) neurons, while simultaneously repressing an
alternative subcortical, GABAergic neuronal phenotype.
Subsequently, later-born (upper-layer) cortical neurons
are specified in an Ngn-independent manner, requiring
instead the synergistic activities of Pax6 and Tlx, which
also control a binary choice between cortical/glutamatergic
and subcortical/GABAergic fates. Our study thus reveals an
unanticipated heterogeneity in the genetic mechanisms
specifying the identity of neocortical projection neurons.
362 citations